Loss of Sprouty2 in human high-grade serous ovarian carcinomas promotes EGF-induced E-cadherin down-regulation and cell invasion

被引：12
|
作者：
So, Wai-Kin [1 ]
Cheng, Jung-Chien [1 ]
Fan, Qianlan [1 ]
Wong, Alice S. T. [2 ]
Huntsman, David G. [3 ,4 ]
Gilks, C. Blake [3 ,5 ,6 ]
Leung, Peter C. K. [1 ]
机构：
[1] Univ British Columbia, Dept Obstet & Gynecol, Child & Family Res Inst, Vancouver, BC V5Z 4H4, Canada
[2] Univ Hong Kong, Sch Biol Sci, Hong Kong, Hong Kong, Peoples R China
[3] Univ British Columbia, BC Canc Agcy, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada
[4] BC Canc Agcy, Dept Mol Oncol, Vancouver, BC, Canada
[5] Vancouver Gen Hosp, Dept Pathol & Lab Med, Vancouver, BC, Canada
[6] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada
来源：
FEBS LETTERS | 2015年 / 589卷 / 03期
基金：
加拿大健康研究院;
关键词：
Sprouty; Epidermal growth factor; E-cadherin; Invasion; Ovarian cancer; GROWTH-FACTOR; SURFACE EPITHELIUM; CANCER; EXPRESSION; INHIBITOR; PROTEIN; SUPPRESSOR; RECEPTOR; HETEROZYGOSITY; METHYLATION;
D O I：
10.1016/j.febslet.2014.12.012
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Sprouty (SPRY) proteins are well-characterized factors that inhibit receptor tyrosine kinase signaling. Our Human Exonic Evidence-Based Oligonucleotide (HEEBO) microarray results showed that the mRNA levels of SPRY2, but not of SPRY1 or SPRY4, are down-regulated in high-grade serous ovarian carcinoma (HGSC) tissues and epithelial ovarian cancer (EOC) cell lines. Molecular inversion probe (MIP) copy number analysis showed the deletion of the SPRY2 locus in HGSC. Overexpression of SPRY2 reduced EGF-induced cell invasion by attenuating EGF-induced E-cadherin down-regulation. Moreover, a positive correlation between SPRY2 and E-cadherin protein levels was observed in HGSC tissues. This study reveals the loss of SPRY2 in HGSC and indicates an important tumor-suppressive role for SPRY2 in mediating the stimulatory effect of EGF on human EOC progression. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：302 / 309
页数：8
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